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Effects of Parecoxib and Fentanyl on nociception-induced cortical activity.

Peng YZ, Li XX, Wang YW - Mol Pain (2010)

Bottom Line: The effects of parecoxib and fentanyl on induced cortical activity were compared.Parecoxib, on the other hand, did not significantly affect the neural activity.Fentanyl showed a strong inhibitory effect on the nociceptive-stimulus induced cortical activity while parecoxib had no significant effect.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Anesthesiology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China.

ABSTRACT

Background: Analgesics, including opioids and non-steroid anti-inflammatory drugs reduce postoperative pain. However, little is known about the quantitative effects of these drugs on cortical activity induced by nociceptive stimulation. The aim of the present study was to determine the neural activity in response to a nociceptive stimulus and to investigate the effects of fentanyl (an opioid agonist) and parecoxib (a selective cyclooxygenase-2 inhibitor) on this nociception-induced cortical activity evoked by tail pinch. Extracellular recordings (electroencephalogram and multi-unit signals) were performed in the area of the anterior cingulate cortex while intracellular recordings were made in the primary somatosensory cortex. The effects of parecoxib and fentanyl on induced cortical activity were compared.

Results: Peripheral nociceptive stimulation in anesthetized rats produced an immediate electroencephalogram (EEG) desynchronization resembling the cortical arousal (low-amplitude, fast-wave activity), while the membrane potential switched into a persistent depolarization state. The induced cortical activity was abolished by fentanyl, and the fentanyl's effect was reversed by the opioid receptor antagonist, naloxone. Parecoxib, on the other hand, did not significantly affect the neural activity.

Conclusion: Cortical activity was modulated by nociceptive stimulation in anesthetized rats. Fentanyl showed a strong inhibitory effect on the nociceptive-stimulus induced cortical activity while parecoxib had no significant effect.

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Changes in EEG, Vm and waveform correlation during nociceptive stimulation. A, left panel: Nociceptive stimulation reduced normalized total power of each EEG band; right panel: The cumulative power probability of the EEG, was shifted to the right, under nociceptive stimulation. B, left panel: The distribution of membrane potential (Vm), was bimodally distributed under the resting condition, and unimodally distributed when nociceptive stimulation was applied; right panel: The cumulative probability of Vm density is plotted before, after and during nocicptive stimulation. All measures returned to pre-stimulation values after nociceptive stimulation was removed. C and D: Waveform correlation between the ACC and S1 showing that the correlation coefficient decreased during tail pinch; in C extracellular recordings were recorded in both regions, in D intracellular recordings were recorded at S1 while extracellular recordings were recorded at ACC. The left panel in both C and D show a sample correlation coefficient before and during nociceptive stimulation. The right panel plots the group data. Each EEG power was normalized to the total power of Pre-stimulation values. The correlation coefficient (peak value near zero seconds) was considerably higher in the resting state than during tail pinch.
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Figure 2: Changes in EEG, Vm and waveform correlation during nociceptive stimulation. A, left panel: Nociceptive stimulation reduced normalized total power of each EEG band; right panel: The cumulative power probability of the EEG, was shifted to the right, under nociceptive stimulation. B, left panel: The distribution of membrane potential (Vm), was bimodally distributed under the resting condition, and unimodally distributed when nociceptive stimulation was applied; right panel: The cumulative probability of Vm density is plotted before, after and during nocicptive stimulation. All measures returned to pre-stimulation values after nociceptive stimulation was removed. C and D: Waveform correlation between the ACC and S1 showing that the correlation coefficient decreased during tail pinch; in C extracellular recordings were recorded in both regions, in D intracellular recordings were recorded at S1 while extracellular recordings were recorded at ACC. The left panel in both C and D show a sample correlation coefficient before and during nociceptive stimulation. The right panel plots the group data. Each EEG power was normalized to the total power of Pre-stimulation values. The correlation coefficient (peak value near zero seconds) was considerably higher in the resting state than during tail pinch.

Mentions: The EEG recordings showed a shift from large-amplitude, low-frequency waves (commonly seen in anaesthetized rats) towards low-amplitude, high-frequency waves (resembling that of awake rats) during tail pinch (Fig. 1A and 1C, upper panels). In addition, the mean firing rate obtained from multi-unit(MU) recordings was enhanced and the Down state disappeared (Fig. 1B). The power spectrum analysis revealed that during tail pinch the ratio of power within low frequency bands was markedly decreased (Fig. 1C), along with the decreased absolute power of each EEG band (Fig. 2A).


Effects of Parecoxib and Fentanyl on nociception-induced cortical activity.

Peng YZ, Li XX, Wang YW - Mol Pain (2010)

Changes in EEG, Vm and waveform correlation during nociceptive stimulation. A, left panel: Nociceptive stimulation reduced normalized total power of each EEG band; right panel: The cumulative power probability of the EEG, was shifted to the right, under nociceptive stimulation. B, left panel: The distribution of membrane potential (Vm), was bimodally distributed under the resting condition, and unimodally distributed when nociceptive stimulation was applied; right panel: The cumulative probability of Vm density is plotted before, after and during nocicptive stimulation. All measures returned to pre-stimulation values after nociceptive stimulation was removed. C and D: Waveform correlation between the ACC and S1 showing that the correlation coefficient decreased during tail pinch; in C extracellular recordings were recorded in both regions, in D intracellular recordings were recorded at S1 while extracellular recordings were recorded at ACC. The left panel in both C and D show a sample correlation coefficient before and during nociceptive stimulation. The right panel plots the group data. Each EEG power was normalized to the total power of Pre-stimulation values. The correlation coefficient (peak value near zero seconds) was considerably higher in the resting state than during tail pinch.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2819047&req=5

Figure 2: Changes in EEG, Vm and waveform correlation during nociceptive stimulation. A, left panel: Nociceptive stimulation reduced normalized total power of each EEG band; right panel: The cumulative power probability of the EEG, was shifted to the right, under nociceptive stimulation. B, left panel: The distribution of membrane potential (Vm), was bimodally distributed under the resting condition, and unimodally distributed when nociceptive stimulation was applied; right panel: The cumulative probability of Vm density is plotted before, after and during nocicptive stimulation. All measures returned to pre-stimulation values after nociceptive stimulation was removed. C and D: Waveform correlation between the ACC and S1 showing that the correlation coefficient decreased during tail pinch; in C extracellular recordings were recorded in both regions, in D intracellular recordings were recorded at S1 while extracellular recordings were recorded at ACC. The left panel in both C and D show a sample correlation coefficient before and during nociceptive stimulation. The right panel plots the group data. Each EEG power was normalized to the total power of Pre-stimulation values. The correlation coefficient (peak value near zero seconds) was considerably higher in the resting state than during tail pinch.
Mentions: The EEG recordings showed a shift from large-amplitude, low-frequency waves (commonly seen in anaesthetized rats) towards low-amplitude, high-frequency waves (resembling that of awake rats) during tail pinch (Fig. 1A and 1C, upper panels). In addition, the mean firing rate obtained from multi-unit(MU) recordings was enhanced and the Down state disappeared (Fig. 1B). The power spectrum analysis revealed that during tail pinch the ratio of power within low frequency bands was markedly decreased (Fig. 1C), along with the decreased absolute power of each EEG band (Fig. 2A).

Bottom Line: The effects of parecoxib and fentanyl on induced cortical activity were compared.Parecoxib, on the other hand, did not significantly affect the neural activity.Fentanyl showed a strong inhibitory effect on the nociceptive-stimulus induced cortical activity while parecoxib had no significant effect.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Anesthesiology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China.

ABSTRACT

Background: Analgesics, including opioids and non-steroid anti-inflammatory drugs reduce postoperative pain. However, little is known about the quantitative effects of these drugs on cortical activity induced by nociceptive stimulation. The aim of the present study was to determine the neural activity in response to a nociceptive stimulus and to investigate the effects of fentanyl (an opioid agonist) and parecoxib (a selective cyclooxygenase-2 inhibitor) on this nociception-induced cortical activity evoked by tail pinch. Extracellular recordings (electroencephalogram and multi-unit signals) were performed in the area of the anterior cingulate cortex while intracellular recordings were made in the primary somatosensory cortex. The effects of parecoxib and fentanyl on induced cortical activity were compared.

Results: Peripheral nociceptive stimulation in anesthetized rats produced an immediate electroencephalogram (EEG) desynchronization resembling the cortical arousal (low-amplitude, fast-wave activity), while the membrane potential switched into a persistent depolarization state. The induced cortical activity was abolished by fentanyl, and the fentanyl's effect was reversed by the opioid receptor antagonist, naloxone. Parecoxib, on the other hand, did not significantly affect the neural activity.

Conclusion: Cortical activity was modulated by nociceptive stimulation in anesthetized rats. Fentanyl showed a strong inhibitory effect on the nociceptive-stimulus induced cortical activity while parecoxib had no significant effect.

Show MeSH
Related in: MedlinePlus